This is an irregular and polymorphic wide complex tachycardia that appears to show a streamer effect, or “turning of the points.”

Is it Torsades de Pointes?

The answer is, it’s impossible to tell from this rhythm strip!

Why?

Because the key distinction between polymorphic VT and Torsades de Pointes (which is a form of polymorphic VT) is that Torsades de Pointes will have a prolonged QT interval in the underlying rhythm!

This rhythm strip doesn’t show the underlying rhythm, so it’s impossible to diagnose as Torsades de Pointes, unless you can derive something useful from the history that would make you reach for the magnesium sulfate instead of the amiodarone (or defibrillator).

Since a normal QT interval varies with heart rate, what we’re really talking about is a prolonged QTc interval (the small ‘c’ stands for ‘corrected’ and normalizes the QT interval for the heart rate).

Most of the books I’ve read suggest that a QTc > 460 ms is prolonged and > 500 ms is clinically significant.

This is an irregular and slightly polymorphic wide complex tachycardia. It’s also very fast! Anytime a tachycardia approaches 250 beats/min., you should be very suspicious of an accessory pathway (or Wolff-Parkinson-White Syndrome).

What else makes this rhythm different from the first? All of the “points” of the QRS complexes are pointing the same direction (in this case down). Familiarize yourself with this rhythm! These patients are rare, but they’re out there!

If you have atrial fibrillation on the monitor, and the shortest R-R interval is 6 small blocks or less, then you should treat it like WPW, and stay away from antiarrhythmics!

Atrial fibrillation in the presence of WPW is a very dangerous rhythm, and one of those occasions where you can kill your patient by selecting the wrong medication. The only safe drug for AF/WPW may be procainamide.

Consider this interesting transcript from Amal Mattu M.D.’s December 2008 podcast at EMedHome.com (thanks for the tip, Maciek!):

Another concern that you need to be aware of is, if you have a patient who has AF with WPW, stay away from amiodarone. Even now, AHA continues to list amiodarone as a viable option, but it’s not a viable option. In fact, the only published reports on using amiodarone in rapid AF and WPW have indicated that amiodarone is associated with adverse outcomes. There’s a handful of case reports of patients that had rapid AF and WPW. They got amiodarone and they decompensated. There are, to my knowledge – and I’ve looked through the literature in detail multiple times – and I have yet to find even a single case report or a single case series or a published study saying, “I had a patient with rapid AF and WPW, I gave him amiodarone, and they did well.” Not a single publication that I can find. The only publications on that particular scenario that have ever been published in the literature are “patient did worse” so my recommendation and a handful of other peoples’ recommendations also; “Stay away from amiodarone if you’re taking care of a patient with rapid AF and WPW.”

Remember the first rule of medicine!

If your patient is hemodynamically stable, then transport the patient to the emergency department for cardioversion. It’s probably the safest option.

Both are polymorphic VT.Torades is a subtype of polymorphic VT. If it’s sustained, it should probably be defibrillated. You’ll note that I said defibrillated and not cardioverted. The computer will have a very difficult time tracking R waves with a polymorphic VT.Most of the time, Torsades will be intermittent, so you’ll have an opportunity to see the underlying rhythm, and consider whether or not a prolonged QTc is present.So, according to the AHA ECC 2005 guidelines for stable irregular wide complex tachycardias, you should consider expert consultation (remember that AF/WPW is a possibility) and give magnesium sulfate for polymorphic VT if the underlying QTc is prolonged, and amiodarone if it is not.You should also attempt to identify the underlying cause of the prolonged QT. For example, hypokalemia, poisoning, prescription drugs, etc.

Ah, I see. The preceding/underlying QTc, of course. Hm. I just got myself a Torsade case that I thought I’d post to the blog. Now I gotta study it closer.. Thanks for thorough and excellent information as always..!

I’m confused as to why the patients who presented with wide-complex tachycardias were treated with adenosine as a first-line medication (especially the irregular ones)…In our system, a patient presenting with stable, regular WCT would be treated with amiodarone as the first medication, while the patient with stable, irregular WCT would usually be assumed to be in AF with some aberrant conduction, and the decision to proceed with cardizem/amiodarone/procainamide would be made in concert with medical control.Perhaps it has to do with the way standing orders are written in NJ, but we automatically bypass adenosine for WCTs as it is only permitted for treatment of narrow-compex tachycardias unless medical control is contacted. It seems pretty darn risky to give WCTs adenosine in the regular treatment pathyway.

Tom, I found this series very interesting, thanks for posting. I especially found the WPW with atrial fib interesting. The links (and other research) says Adenosine causes v. fib, and cardizem causes a faster rate.
In the PA protocols, we give cardizem for a stable irregular narrow complex tachycardia (need to call med command first). For a stable irregular wide complex tachycardia, we give amioderone (again, have to call medical command first). Lidocaine's only indicated for a stable regular wide complex tachycardia, but it's still written to "try amioderone first." I also don't recall ever being taught about this dangerous condition in classes. Following our protocols could make the patient condition much worse, so I think more attention should be brought to this issue.

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Vince DiGiulio59 Year Old Female: Intermittent Head Pain (Conclusion)Thanks! There's a couple of reasons why V7-9 might have been negative here: 1) Not all "inferoposterior" STEMI's show ST-elevation in V7-V9. Sometimes the ST-depression we see in V2 and V3 is reciprocal to the inferior STEMI and not really caused by posterior injury. 2) You'll notice that there is only subtle ST-depression in V3…
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